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In Reply:-I appreciate the interest in our article [1] expressed by Harrop-Griffiths and Hood. They have some comments on the methods of our study and on the possible mechanisms behind the phenomenon we describe in our results.

First, studying an additional crossover group may have a real theoretical, but not much clinical, interest. In clinical practice, pancuronium is very seldom administered after mivacurium.

Second, although we were indeed aware of the article by Feldman et al., [2] we believe our speculation was justified. Harrop-Griffiths and Hood suggest that the first relaxant given dominates also the action of the second one in the biophase, which, in this case, is the same as at the neuromuscular junction. Generally, we agree with this opinion, and presented it in our discussion as the first explanation for the interaction between pancuronium and mivacurium. However, in this particular case, it is difficult to imagine that so small a dose of mivacurium (10 micro gram/kg) after pancuronium could have such a long-lasting effect without some special mechanism. As we stated, we did not study the underlying mechanism, but theorized an explanation for this significant interaction. Therefore, and because there also are supporting aspects [3,4] for this opinion, we suggested pancuronium's capacity to inhibit pseudocholinesterase as only one possible explanation for our observation.